Bicycling but not Walking Is Independently Associated With Fasting Insulin in Abdominally Obese Women

2011 ◽  
Vol 8 (6) ◽  
pp. 820-823 ◽  
Author(s):  
Erik Hemmingsson ◽  
Ulf Ekelund ◽  
Joanna Udden
Keyword(s):  
Insulin Resistance ◽  
Body Fat ◽  
Abdominal Obesity ◽  
Serum Insulin ◽  
Whole Body ◽  
Obese Women ◽  
Fasting Serum ◽  
Insulin Levels ◽  
The Impact

Background:The impact of walking and bicycling on insulin resistance (IR) in women with abdominal obesity is unclear.Methods:Pooled analysis of data from a randomized trial on physically active commuting (bicycling + walking vs walking only) in women with abdominal obesity [n = 98; age:47.3 ± 7.6 yrs; waist circumference (WC):103.1 ± 7.8 cm]. Bicycling and walking data were collected during 7 consecutive days by trip meters (Trelock FC-410) and pedometers (Yamax digiwalker SW-200) at baseline, 2, 4, and 6 months. Owing to a skew distribution we analyzed bicycling as a binary dummy variable with a 10 km/week cut-off. Fasting serum insulin and homeostatic model assessment – insulin resistance (HOMA-IR) were assessed at baseline and 6 months, as were body mass index (BMI), WC, and dual x-ray absorptiometry (DXA)-assessed % whole-body fat.Results:Increased bicycling by 10 km/wk was associated with reductions in fasting serum insulin at follow-up independent of age, treatment allocation, baseline phenotype, Δ walking, and Δ % body fat (β = −10.9, P = .042), but not HOMA-IR (β = −2.0, P = .13). Increased walking was not associated with fasting serum insulin (P = .33) or HOMA-IR (P = .44) at follow-up, after adjustment for the same covariates and Δ bicycling.Conclusion:Increased bicycling but not walking was associated with reduced insulin levels at follow-up. Bicycling may be more effective than walking for reducing insulin levels in abdominally obese women.

scholarly journals The Effect of Short Term Aerobic Training on Serum Insulin and Insulin Resistance in Adult Obese Females

2020 ◽  
Author(s):  
Ashraf Amini ◽  
Zahra Mirakhori ◽  
Mojtaba Eizadi
Keyword(s):  
Insulin Resistance ◽  
Aerobic Training ◽  
Fasting Glucose ◽  
Serum Insulin ◽  
Exercise Group ◽  
P Value ◽  
Obese Women ◽  
Fat Percentage ◽  
Short Term ◽  
The Impact

Objective: Obesity is associated with inflammatory process and many different diseases. The objective of this study was to assess the impact of short term aerobic training on serum resistin and insulin resistance in adult obese women. Materials and Methods: In this quasi-experimental study, thirty untrained adult obese females matched for age 35-45 years old with body mass index (BMI) 30-36 kg/m2 were divided randomly into exercise (aerobic intervention; 6 weeks, 3 days/weekly, %55-70HRmax) and control (no training) groups. Pre and post-training of fasting blood samples were collected for measure serum resistin. Insulin resistance was calculated by HOMA-IR. Data were analyzed by the independent samples T-test. Results: Aerobic training resulted in significant decrease in BMI (32.1 (± 2.76) vs 31.6 (± 2.80) kg/m2, P-value: 0.023), body fat percentage (44.7 (± 4.55) vs 44 (± 4.33), P-value: 0.028) and fasting glucose (94 (± 8.9) vs 79 (± 5.8) mg/dl, P-value: 0.011) in exercise group. No changes were observed on insulin resistance (1.43 (± 1.11) vs 1.18 (± 0.57) HOMA-IR, P-value: 0.124) and serum resistin (2.20 (± 1.07) vs 1.58 (± 0.87) ng/ml P-value: 0.062) by training program. All variables remained unchanged in control subjects. Conclusion: Despite improving fasting glucose, a short-term aerobic training is not associated with anti-inflammatory property for obese females. Improved glucose could be likely attributed to other changes in metabolic markers in response to exercise training and further studies are necessary to clarify possible mechanisms

scholarly journals Fasting serum insulin levels and insulin resistance are associated with colorectal adenoma in Koreans

2013 ◽  
Vol 5 (3) ◽  
pp. 297-304 ◽  
Author(s):  
Eun Hee Kim ◽  
Hong-Kyu Kim ◽  
Sung Jin Bae ◽  
Hye-Sook Chang ◽  
Hye Won Park ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Colorectal Adenoma ◽  
Serum Insulin ◽  
Fasting Serum ◽  
Insulin Levels

scholarly journals Short-term high-fat feeding induces islet macrophage infiltration and β-cell replication independently of insulin resistance in mice

2016 ◽  
Vol 311 (4) ◽  
pp. E763-E771 ◽  
Author(s):  
David C. Woodland ◽  
Wei Liu ◽  
Jacky Leong ◽  
Mallory L. Sears ◽  
Ping Luo ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Blood Glucose ◽  
Serum Insulin ◽  
Cell Replication ◽  
Fat Pad ◽  
High Fat ◽  
Fasting Serum ◽  
Β Cell ◽  
Short Term ◽  
Insulin Levels

Short-term high-fat consumption stimulates mouse islet β-cell replication through unknown mechanisms. Resident macrophages (MΦs) are capable of secreting various factors involved in islet development and tissue remodeling. We hypothesized that a short-term high-fat diet (HFD) promotes MΦ infiltration in pancreatic islets and that MΦs serve as a regulator of β-cell replication. To test these hypotheses and dissect mechanisms involved in HFD-induced β-cell replication, adult C57BL/6J mice were fed a HFD for 7 days with or without administration of clodronate-containing liposomes, an MΦ-depleting agent. Mouse body and epididymal fat pad weights, and nonfasting blood glucose and fasting serum insulin levels were measured, and pancreatic islet β-cell replication, oxidative stress, and MΦ infiltration were examined. Short-term HFD promoted an increase in body and epididymal fat pad weight and blood glucose levels, along with an increased fasting serum insulin concentration. β-Cell replication, islet MΦ infiltration, and the percentage of inducible NO synthase positive MΦs in the islets increased significantly in mice fed the HFD. Immunofluorescence staining for 8-oxo-2′-deoxyguanosine or activated caspase-3 revealed no significant induction of DNA damage or apoptosis, respectively. In addition, no change in stromal-derived factor 1-expressing cells was found induced by HFD. Despite continuous elevation of nonfasting blood glucose and fasting serum insulin levels, depletion of MΦs through treatments of clodronate abrogated HFD-induced β-cell replication. These findings demonstrated that HFD-induced MΦ infiltration is responsible for β-cell replication. This study suggests the existence of MΦ-mediated mechanisms in β-cell replication that are independent of insulin resistance.

scholarly journals Fasting serum insulin levels and insulin resistance are associated with blood rheology in Japanese young adults without diabetes

2016 ◽  
Vol 44 (3) ◽  
pp. 496-507 ◽  
Author(s):  
Kensuke Yoshida ◽  
Takao Kimura ◽  
Tomoyuki Aoki ◽  
Katsuhiko Tsunekawa ◽  
Osamu Araki ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Young Adults ◽  
Serum Insulin ◽  
Blood Rheology ◽  
Fasting Serum ◽  
Insulin Levels

scholarly journals Insulin Resistance Induced by Maximal Exercise Correlates With a Post-Exercise Increase in Uridine Concentration in the Blood of Healthy Young Men

2013 ◽  
pp. 163-170 ◽  
Author(s):  
W. DUDZINSKA ◽  
A. LUBKOWSKA ◽  
K. JAKUBOWSKA ◽  
M. SUSKA ◽  
E. SKOTNICKA
Keyword(s):  
Insulin Resistance ◽  
Insulin Sensitivity ◽  
Healthy Subjects ◽  
Maximal Exercise ◽  
Serum Insulin ◽  
Model Assessment ◽  
Post Exercise ◽  
Insulin Levels ◽  
Exercise Induced ◽  
The Impact

Uridine is postulated to participate in the development of insulin resistance. Since exercise is an effective tool in the treatment of insulin resistance it appeared justified to assess the impact of maximal exercise on plasma uridine and insulin sensitivity indices (e.g. insulin and HOMA-IR) in healthy subjects. The study included forty-four healthy males (18.5±2.92 years, VO2max 50.2±6.26 ml kg-1 min-1). Subjects performed a single maximal exercise on a bicycle ergometer. Blood samples were taken three times: immediately before exercise, immediately after exercise and at the 30th min of rest. Uridine concentrations were determined in the whole blood using high-performance liquid chromatography. Serum insulin levels were measured by a specific ELISA method. Insulin sensitivity was assessed by homeostasis model assessment method (HOMA-IR). A maximal exercise-induced increase in the concentration of uridine correlated with post-exercise increases in insulin levels and HOMA-IR. Our results indicate a relationship between the concentration of uridine in the blood and indicators of insulin sensitivity in healthy subjects. We are the first to demonstrate that a maximal exercise-induced increase in the concentration of uridine is correlated with post-exercise increases in insulin levels and HOMA-IR in healthy subjects. It appears that uridine may be an indicator of insulin resistance.

Comparative effectiveness of carvedilol and propranolol on glycemic control and insulin resistance associated with l-thyroxin-induced hyperthyroidism — an experimental study

2007 ◽  
Vol 85 (5) ◽  
pp. 514-520 ◽  
Author(s):  
Parloop Bhatt ◽  
Dharmesh Makwana ◽  
Devdas Santani ◽  
Ramesh Goyal
Keyword(s):  
Insulin Resistance ◽  
Blood Pressure ◽  
Heart Rate ◽  
Body Mass ◽  
Serum Insulin ◽  
Area Under The Curve ◽  
Serum Glucose ◽  
Fasting Serum ◽  
Insulin Levels ◽  
Propranolol Treatment

The present study was undertaken to investigate the effectiveness of adrenergic antagonists carvedilol and propranolol on l-thyroxin-induced cardiovascular and metabolic disturbances in rats. Treatment with l-thyroxin sodium (75 mg/kg body mass, s.c., every alternate day for 3 weeks), produced a significant increase in food and water intake, body temperature, heart rate, systolic blood pressure, along with an increase in serum T3, T4, and triglyceride levels. Besides a significant reduction in body mass, serum levels of TSH and cholesterol were also reduced following l-thyroxin treatment. Carvedilol (10 mg/kg body mass, orally) and propranolol (10 mg/kg body mass, i.p.) administered daily in the third week to 2 separate groups of l-thyroxin-treated animals reversed thyroxin-induced loss in body mass and rise in body temperature, blood pressure, and heart rate. Propranolol treatment increased TSH levels and decreased T3 and T4 levels in hyperthyroid animals, whereas carvedilol did not produce any effect on thyroid hormones. Carvedilol treatment reversed thyroxin induced hypertriglyceridemia, whereas propranolol treatment had no effect. Both carvedilol and propranolol prevented decrease in cholesterol levels induced by thyroxine. Compared with normal animals, l-thyroxin-treated animals showed a state of hyperglycemia, hyperinsulinaemia, impaired glucose tolerance, and insulin resistance, as inferred from elevated fasting serum glucose and insulin levels, higher area under the curve over 120 min for glucose, and decreased insulin sensitivity index (KITT). Propranolol and carvedilol treatment significantly decreased fasting serum glucose levels. Treatment with propranolol did not alter serum insulin levels, area-under-the-curve glucose, or KITT values. However, treatment with carvedilol significantly reduced area-under-the-curve glucose, decreased fasting serum insulin levels and significantly increased KITT values. In conclusion, carvedilol appears to produce favorable effects on insulin sensitivity and glycemic control and can therefore be considered as more efficacious adjunctive treatment than propranolol in hyperthyroidism.

scholarly journals The activity of the pyruvate dehydrogenase complex in heart and liver from mice during the development of obesity and insulin resistance

1987 ◽  
Vol 243 (2) ◽  
pp. 549-553 ◽  
Author(s):  
I D Caterson ◽  
L D Astbury ◽  
P F Williams ◽  
M A Vanner ◽  
G J Cooney ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Pyruvate Dehydrogenase ◽  
Serum Insulin ◽  
Pyruvate Dehydrogenase Complex ◽  
Active Form ◽  
Whole Body ◽  
Acid Oxidation ◽  
Mitochondrial Fatty Acid Oxidation ◽  
Gold Thioglucose ◽  
Mitochondrial Fatty Acid

The amount of pyruvate dehydrogenase in the active form (PDHa) was increased 1.7-fold compared with controls in heart muscle of mice 1 week after induction of obesity with a single injection of gold-thioglucose. At 4 weeks post injection, the amount of PDHa was decreased to 32% of control, a value which was observed in later stages of the obesity syndrome. In contrast, liver PDHa was increased and remained at an increased activity during the development of obesity. Despite normal post-prandial serum insulin contents, liver membrane insulin-receptor numbers were decreased 1 week after gold-thioglucose injection, and there was no change in receptor affinity. The decrease in heart PDHa in the obese animals was reversed by a single dose of 2-tetradecylglycidic acid, but this inhibitor of mitochondrial fatty acid oxidation did not affect liver PDHa in these animals. These early and diverse changes in PDHa argue for a multifactorial aetiology in the development of the whole-body insulin resistance seen in older gold-thioglucose-treated obese animals.

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